Infection of wounds is a major source of healthcare expenditure in the United States. Approximately 5% of all surgical wounds become infected with microorganisms, and that figure is considerably higher (10-20%) for patients undergoing abdominal surgery. Colonization rates are significantly higher in the hospital setting, both among healthcare workers, and among patients. Moreover, the colonizing organisms in the hospital environment are likely to be resistant to many forms of anti-microbial therapy, due to the strong selective pressure that exists in the nosocomial environment, where antibiotics are frequently used. For example, Staphylococci are usually carried as harmless commensals, however given a breach in the epidermis, they can cause severe, even life threatening infection in the human host.
Anti-microbial host defense peptides have been recognized as effector molecules of the innate immune system that are considered integral to the first line of defense to fight microbial infections. Such anti-microbial peptides are widely distributed among species. These peptides are characterized by cationic properties that facilitate interactions with the negatively charged phospholipids of the bacterial membrane. Anti-microbial peptides have been shown to kill by permeabilizing the membrane of microbial organisms. For example, it has been shown that defense peptide molecules can aggregate and form voltage dependent channels in the lipid bilayer resulting in the permeabilization of both the inner and outer membrane of the microorganism (Lehrer, R. I., J. Clin. Investigation., 84:553 (1989)). The amphiphilic nature of these molecules facilitates the insertion of the hydrophobic residue into the lipid bilayer by electrostatic attraction while the polar residues project into and above the membrane.
Resistance to anti-microbial peptides is one of the key virulence factors of a successful pathogen. Pathogenic microorganisms have evolved several mechanisms by which they counteract the anti-microbial effect of these peptides. These include (i) covalent modifications of anionic molecules to reduce the negative charge of the bacterial cell envelope (ii) efflux of anti-microbial peptides via the proton-motive-force dependent efflux pumps (iii) alteration of the membrane fluidity and (iv) inactivation of anti-microbial peptides by proteolytic cleavage. These mechanisms of peptide resistance lead to the establishment of infection in the host.
The most common way of preventing microbial infection is to administer prophylactic antibiotic drugs. While generally effective, this strategy has the unintended effect of breeding resistant strains of bacteria. The routine use of prophylactic antibiotics should be discouraged for the very reason that it is encouraging the growth of resistant strains
Rather than using routine prophylaxis, a better approach is to practice good wound management, i.e., keep the area free from bacteria before, during, and after surgery, and carefully monitor the wound site for infection during healing. Normal monitoring methods include close observation of the wound site for slow healing, signs of inflammation and pus, as well as measuring the patient's temperature for signs of fever. Unfortunately, many symptoms are only evident after the infection is already established. Furthermore, after a patient is discharged from the hospital they become responsible for monitoring their own healthcare, and the symptoms of infection may not be evident to the unskilled patient.
A system or biosensor that can detect the early stages of infection before symptoms develop would be advantageous to both patients and healthcare workers. If a patient can accurately monitor the condition of a wound after discharge, then appropriate anti-microbial therapy can be initiated early enough to prevent a more serious infection.